Journal article
Atypical chemokine receptor 4 shapes activated B cell fate
Ervin E Kara, Cameron R Bastow, Duncan R McKenzie, Carly E Gregor, Kevin A Fenix, Rachelle Babb, Todd S Norton, Dimitra Zotos, Lauren B Rodda, Jana R Hermes, Katherine Bourne, Derek S Gilchrist, Robert J Nibbs, Mohammed Alsharifi, Carola G Vinuesa, David M Tarlinton, Robert Brink, Geoffrey R Hill, Jason G Cyster, Iain Comerford Show all
Journal of Experimental Medicine | ROCKEFELLER UNIV PRESS | Published : 2018
DOI: 10.1084/jem.20171067
Abstract
Activated B cells can initially differentiate into three functionally distinct fates-early plasmablasts (PBs), germinal center (GC) B cells, or early memory B cells-by mechanisms that remain poorly understood. Here, we identify atypical chemokine receptor 4 (ACKR4), a decoy receptor that binds and degrades CCR7 ligands CCL19/CCL21, as a regulator of early activated B cell differentiation. By restricting initial access to splenic interfollicular zones (IFZs), ACKR4 limits the early proliferation of activated B cells, reducing the numbers available for subsequent differentiation. Consequently, ACKR4 deficiency enhanced early PB and GC B cell responses in a CCL19/CCL21-dependent and B cell-intr..
View full abstractGrants
Awarded by Australian National Health and Medical Research Council
Awarded by NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
Funding Acknowledgements
This work was supported in part by a grant from the Australian National Health and Medical Research Council (APP1105312) to S.R. McColl, J.G. Cyster, and I. Comerford, J.G. Cyster is an investigator of the Howard Hughes Medical Institute. E.E. Kara is supported by an Australian postgraduate award, a Norman and Patricia Polglase scholarship, and a National Health and Medical Research Council C.J. Martin Overseas Biomedical fellowship.